Share this story

Dr Michael Zasloff is a professor, medical researcher, immunologist and geneticist and is currently professor of surgery and paediatrics at Georgetown University School of Medicine, US. In 1993 he discovered squalamine in the liver tissue of dogfish sharks. Between 2002 and 2004 he served as Dean of Research and Translational Science for Georgetown University School of Medicine.

We found evidence that squalamine slows down the formation of the toxins associated with Parkinson’s

Dr Christopher Dobson

Steroid in shark livers could hold key to Parkinson’s treatment

Advances

Author: Almaz OhenePublished: 18 January 2017

Prep: Cook: Serves:

New research suggests that a naturally occurring substance called squalamine, found in the livers of dogfish sharks, could help treat Parkinson’s disease

A steroid found in the livers of dogfish sharks could help treat Parkinson’s disease, scientists at the University of Cambridge, UK, believe.

The natural compound, called squalamine, is often studied for its anti-cancer and anti-infective properties but researchers now think that it could also lead to future treatments for Parkinson’s disease.

Dr Michael Zasloff, professor of surgery and paediatrics at Georgetown University School of Medicine, co-authored a recent research paper published in ‘Proceedings of the National Academy of Sciences’ that suggests squalamine dramatically inhibits the early formation of toxic aggregates of the protein alpha-synuclein, which is thought to start a chain reaction of molecular events eventually leading to the development of Parkinson’s.

The research team also found that squalamine could suppress the toxicity of these poisonous particles in worms. Dr Zasloff said: “We could literally see that the oral treatment of squalamine did not allow alpha-synuclein to cluster, and prevented muscular paralysis inside the worms.”

Dr Christopher Dobson, chemistry professor at the University of Cambridge and one of the paper’s co-authors, said: “To our surprise, we found evidence that squalamine not only slows down the formation of the toxins associated with Parkinson’s disease, but also makes them less toxic altogether.”

Scientists from the Italy, the Netherlands, Spain, the UK and the US all worked together to make this discovery. The team assert that it is scientifically possible for squalamine to prevent the progression of the condition; but advise that individuals with late-stage Parkinson’s – after many of the areas of the brain have been destroyed – will not benefit from the treatment’s in the same way as those whereby treatment would begin sooner.

The team would like to conduct further research to determine what the precise benefits of squalamine would be – and what form any resulting drug might take.

This video shows what happens if the worms are fed squalamine as they develop: they have much more movement.

About squalamine

The anti-microbial compound was discovered in 1993 by Dr Michael Zasloff in the liver tissue of dogfish sharks. He was looking for an explanation as to why the fish were so good at fighting off infection. Scientists can now create a synthetic form of the compound in the laboratory.

Share this story

Dr Michael Zasloff is a professor, medical researcher, immunologist and geneticist and is currently professor of surgery and paediatrics at Georgetown University School of Medicine, US. In 1993 he discovered squalamine in the liver tissue of dogfish sharks. Between 2002 and 2004 he served as Dean of Research and Translational Science for Georgetown University School of Medicine.

We found evidence that squalamine slows down the formation of the toxins associated with Parkinson’s

IN THE NEWS

Carefully selected news stories from the international Parkinson's community.

3 weeks ago

Excess calcium in brain could cause Parkinson’s

Researchers at the University of Cambridge, UK, have discovered that excess levels of calcium in brain cells may lead to the formation of the toxic clusters that signify Parkinson’s disease. The findings, reported in the journal ‘Nature Communications’, show that calcium can influence the interaction between small membranous structures inside nerve endings, which are important for neuronal signaling in the brain, and alpha-synuclein – the protein associated with Parkinson’s disease. Dr Janin Lautenschläger, the paper’s first author, said: “This is the first time we’ve seen that calcium influences the way alpha-synuclein interacts with synaptic vesicles. We think that alpha-synuclein is almost like a calcium sensor. In the presence of calcium, it changes its structure and how it interacts with its environment, which is likely very important for its normal function.”

Jewish people with Crohn’s disease more likely to carry LRRK2 gene mutation

A scientific study has concluded that there may be a link between Parkinson’s and Crohn’s disease within the Ashkenazi Jewish community. The study’s findings, which were published in the journal ‘Science Translational Medicine’, has found that members of the population with Crohn’s disease are more likely to carry the LRRK2 mutation which is a significant cause of Parkinson’s. Lead researcher Dr Inga Peter, professor of genetics and genomic sciences at the Icahn School of Medicine, New York, US, said: “Crohn’s disease is a complex disorder with multiple genes and environmental factors involved, which disproportionately affects individuals of Ashkenazi Jewish ancestry. “The presence of shared LRRK2 mutations in patients with Crohn’s disease and Parkinson’s disease provides refined insight into disease mechanisms and may have major implications for the treatment of these two seemingly unrelated diseases.”

Could caffeine in the blood help diagnose Parkinson’s?

Blood caffeine levels could be promising diagnostic biomarkers for early-stage Parkinson’s, Japanese researchers reported in the journal ‘Neurology’ earlier this month. The study found that people with Parkinson’s had lower levels of caffeine and caffeine metabolites in their blood than people without the disease, at the same consumption rate. Caffeine concentrations also were decreased in Parkinson’s patients with motor fluctuations than in those without Parkinson’s. However, patients in more severe disease stages did not have lower caffeine levels. The study’s authors, Dr David Munoz, University of Toronto, and Dr Shinsuke Fujioka, Fukuoka University, suggested that the “decrease in caffeine metabolites occurs from the earliest stages of Parkinson’s.” They added: “If a future study were to demonstrate similar decreases in caffeine in untreated patients with Parkinson’s […] the implications of the current study would take enormous importance.”